eMedicine Specialties > Cardiology > Pericardial Disease

Pericardial Effusion: Differential Diagnoses & Workup

Author: William J Strimel, DO, Fellow, Cardiovascular Disease, Scott and White Memorial Hospital
Coauthor(s): Ramin Assadi, MD, Staff Physician, Department of Internal Medicine, Loma Linda University; Ali A Sovari, MD, Research Fellow, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA); Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago
Contributor Information and Disclosures

Updated: Sep 9, 2008

Differential Diagnoses

Cardiac Tamponade
Pericarditis, Constrictive-Effusive
Cardiomyopathy, Dilated
Pericarditis, Uremic
Myocardial Infarction
Pulmonary Edema, Cardiogenic
Myocardial Ischemia
Pulmonary Embolism
Pericarditis, Acute
Pericarditis, Constrictive

Workup

Laboratory Studies

The following lab studies may be performed in patients with suspected pericardial effusion.

  • Electrolytes - Metabolic abnormalities (eg, renal failure)
  • CBC count with differential - Leukocytosis for evidence of infection, as well as cytopenias, as signs of underlying chronic disease (eg, cancer, HIV)
  • Cardiac enzymes: Troponin level is frequently minimally elevated in acute pericarditis, usually in the absence of an elevated total creatine kinase level. Presumably, this is due to some involvement of the epicardium by the inflammatory process. Although the elevated troponin may lead to the misdiagnosis of acute pericarditis as a myocardial infarction, most patients with an elevated troponin and acute pericarditis have normal coronary angiograms. An elevated troponin level in acute pericarditis typically returns to normal within 1-2 weeks and is not associated with a worse prognosis.
  • Thyroid-stimulating hormone - Thyroid-stimulating hormone screen for hypothyroidism
  • Rickettsial antibodies - If high index of suspicion of tick-borne disease
  • Rheumatoid factor, immunoglobulin complexes, antinuclear antibody test (ANA), and complement levels (which would be diminished) - In suspected rheumatologic causes
  • Pericardial fluid analysis - Routine tests
    • Lactic (acid) dehydrogenase (LDH), total protein - The Light criteria (for exudative pleural effusion) found to be as reliable in distinguishing between exudative and transudative effusions
      • Total protein fluid-to-serum ratio >0.5
      • LDH fluid-to-serum ratio >0.6
      • LDH fluid level exceeds two thirds of upper-limit of normal serum level
    • Other indicators suggestive of exudate - Specific gravity >1.015, total protein >3.0 mg/dL, LDH >300 U/dL, glucose fluid-to-serum ratio <1
    • Cell count - Elevated leukocytes (ie, >10,000) with neutrophil predominance suggests bacterial or rheumatic cause, although unreliable
    • Gram stain - Specific but insensitive indicator of bacterial infection
    • Cultures - Signals and identifies infectious etiology
    • Fluid hematocrit for bloody aspirates - Hemorrhagic fluid hematocrits usually significantly less than simultaneous peripheral blood hematocrits
  • Pericardial fluid - Special tests
    • Viral cultures
    • Adenosine deaminase; polymerase chain reaction (PCR); culture for tuberculosis; smear for acid-fast bacilli in suspected tuberculosis infection, especially in patients with HIV
    • A definite diagnosis of tuberculous pericarditis is based on the demonstration of tubercle bacilli in pericardial fluid or on a histological section of the pericardium. Probable tuberculous pericarditis is based on the proof of tuberculosis elsewhere in a patient with otherwise unexplained pericarditis, a lymphocytic pericardial exudate with elevated adenosine deaminase levels, and/or appropriate response to a trial of antituberculosis chemotherapy.

Imaging Studies

Chest radiography

  • Findings include enlarged cardiac silhouette (so-called water-bottle heart), pericardial fat stripe (see Media file 1).
  • A third of patients have a coexisting pleural effusion.
  • Radiography is unreliable in establishing or refuting diagnosis of pericardial effusion.  
Echocardiogram
  • Echocardiography is the imaging modality of choice for the diagnosis of pericardial effusion. Most importantly, the contribution of pericardial effusion to overall cardiac enlargement and the relative roles of tamponade and myocardial dysfunction to altered hemodynamics can be evaluated with echocardiography.6 (See Media file 2.)
  • Pericardial effusion appears as an "echo-free" space between the visceral and parietal pericardium (see Media file 3). Early effusions tend to accumulate posteriorly owing to expandable posterior/lateral pericardium. Large effusions are characterized by excessive motion within the pericardial sac. Severe cases may be accompanied by diastolic collapse of the right atrium and right ventricle (and in hypovolemic patients the left atrium and left ventricle), signaling the onset of pericardial tamponade (see Cardiac Tamponade).
  • Pericardial effusions are described as small, moderate, or large based on the size of the echo-free space seen between the parietal and visceral pleurae on 2-dimensional echocardiography. Small effusions have an echo-free space of less than 5 mm, and are generally seen posteriorly. Moderate-sized effusions range from 5-10 mm and are circumferential, and greater than 10 mm indicates a large effusion. Fluid adjacent to the right atrium is an early sign of pericardial effusion.7
  • False-positive echocardiograms can occur in pleural effusions, pericardial thickening, increased epicardial fat tissue, atelectasis, and mediastinal lesions.
  • Epicardial fat tissue is more prominent anteriorly but may appear circumferentially, thus mimicking effusion. Fat is slightly echogenic and tends to move in concert with the heart, 2 characteristics that help distinguish it from an effusion, which is generally echolucent and motionless.6
  • In addition to its mimicry, pericardial fat accumulation is a source of bioactive molecules, is significantly associated with obesity-related insulin resistance, and may be a coronary risk factor.8,9
  • In patients with pericardial effusion, imaging from low to midposterior thorax can provide additional diagnostic echocardiographic images and should be used in patients in whom conventional images are technically difficult or require additional information. 
Transesophageal echocardiography (TEE)
  • TEE is useful in characterizing loculated effusions, but may be difficult to perform in patients with symptomatic effusions.
Computed tomography
  • CT can potentially determine composition of fluid and may detect as little as 50 mL of fluid.
  • CT can detect pericardial calcifications, which can be indicative of constrictive pericarditis.
  • CT results in fewer false-positive results than echocardiography.
  • CT can be problematic in patients who are unstable given the time required to transport to and from the scanner and perform the test. 
Magnetic resonance imaging
  • MRI can detect as little as 30 mL of pericardial fluid.
  • May be able to distinguish hemorrhagic and no hemorrhagic fluids, as hemorrhagic fluids have a high signal intensity on T-1 weighted images, whereas no hemorrhagic fluids have a low signal intensity.
  • Nodularity or irregularity of the pericardium seen on MRI may be indicative of a malignant effusion.
  • MRI is more difficult to perform than CT scan acutely, given the length of time the patient must remain in the scanner.
Both MRI and CT scan may be superior to echocardiography in detecting loculated pericardial effusions, especially when located anteriorly. Also, these modalities allow for greater visualization of the thoracic cavity and adjacent structures, and therefore may identify other abnormalities relating to the cause of the effusion.
 

Other Tests

Electrocardiography

  • Early in the course of acute pericarditis, the ECG typically displays diffuse ST elevation in association with PR depression. The ST elevation is usually present in all leads except for aVR, but postmyocardial infarction pericarditis, the changes may be more localized. Classically, the ECG changes of acute pericarditis evolve through 4 progressive stages (see Media file 4):
    • Stage I - Diffuse ST-segment elevation and PR-segment depression
    • Stage II - Normalization of the ST and PR segments
    • Stage III - Widespread T-wave inversions
    • Stage IV - Normalization of the T waves
  • Patients with uremic pericarditis frequently do not have the typical ECG abnormalities.

Procedures

  • Pericardiocentesis
    • This procedure is used for diagnostic as well as therapeutic purposes. Support for the use of echocardiographic guidance is increasing, unless emergent treatment is required.
    • Indications include impending hemodynamic compromise (ie, pericardial tamponade), suspected infectious etiology, and uncertain etiology.
    • Use of a needle that is at least 5 cm long, 16-gauge in diameter, and has a short bevel can minimize the risk of complications and should allow for adequate pericardial drainage. A system allowing placement of a catheter over the needle is preferred.
    • Contrast echocardiography using agitated saline is useful in cases when bloody fluid is aspirated to determine if the needle is in the ventricular cavity.
    • Attaching an ECG electrode to the pericardiocentesis needle is also useful for avoiding myocardial puncture. Electrical activity will be seen on the monitor when the needle comes into contact with atrial or ventricular myocardium. These changes may be delayed, however, and instill a false sense of security in needle placement; sense of touch and the findings on aspiration should guide the procedure, with the clinician ultimately relying on good clinical sense.
    • Complications of pericardiocentesis include ventricular rupture, dysrhythmias, pneumothorax, myocardial and/or coronary artery laceration, and infection.
    • Recurrence rates within 90 days may be as high as 90% in patients with cancer.
  • Balloon pericardotomy
    • A catheter is placed in the pericardial space under fluoroscopy, which, after inflation of the balloon, creates a channel for passage of fluid into the pleural space, where reabsorption occurs more readily.
    • This may be useful for recurrent effusions.
  • Pericardial sclerosis
    • Several pericardial sclerosing agents have been used with varying success rates (eg, tetracycline, doxycycline, cisplatin, 5-fluorouracil).
    • The pericardial catheter may be left in place for repeat instillation if necessary until the effusion resolves.
    • Complications include intense pain, atrial dysrhythmias, fever, and infection.
    • Success rates are reported as high as 91% at 30 days.
  • Pericardioscopy
    • This procedure is not universally available.
    • It may increase diagnostic sensitivity in cases of unexplained pericardial effusions. It allows for visualization of pericardium and for pericardial biopsies.

More on Pericardial Effusion

Overview: Pericardial Effusion
Differential Diagnoses & Workup: Pericardial Effusion
Treatment & Medication: Pericardial Effusion
Follow-up: Pericardial Effusion
Multimedia: Pericardial Effusion
References
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Further Reading

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Keywords

pericardial effusion, pericardial sac, dropsy of pericardium, pericarditis, pericardial tamponade, pericardiocentesis, pericardioscopy, malignant pericardial effusion, leukemia, lymphoma, idiopathic effusions, Beck triad of pericardial tamponade, hypotension, muffled heart sounds, jugular venous distension

pulsus paradoxus, pericardial friction rub, hepatojugular reflux, Ewart sign, hepatosplenomegaly, cyanosis, hydropericardium, congestive heart failure, valvular disease, mediastinal lymphoma, Hodgkin disease, metastatic breast cancer, bacterial pericardial effusion, viral pericardial effusion, tuberculous pericardial effusion, parasitic pericardial effusion, HIV-related pericardial effusion, fungal pericardial effusion, systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, vasculitides, uremia, postpericardiotomy syndrome, chylopericardium, myxedema, radiation-induced pericardial effusion

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Contributor Information and Disclosures

Author

William J Strimel, DO, Fellow, Cardiovascular Disease, Scott and White Memorial Hospital
William J Strimel, DO is a member of the following medical societies: American College of Cardiology, American College of Physicians, and Society of Hospital Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Ramin Assadi, MD, Staff Physician, Department of Internal Medicine, Loma Linda University
Ramin Assadi, MD is a member of the following medical societies: American College of Physicians and American Medical Association
Disclosure: Nothing to disclose.

Ali A Sovari, MD, Research Fellow, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA)
Ali A Sovari, MD is a member of the following medical societies: American College of Physicians, American Heart Association, and American Medical Association
Disclosure: Nothing to disclose.

Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago
Abraham G Kocheril, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, Cardiac Electrophysiology Society, Central Society for Clinical Research, Heart Failure Society of America, Heart Rhythm Society, and Illinois State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Justin D Pearlman, MD, PhD, ME, MA, Director of Dartmouth Advanced Imaging Center, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center
Justin D Pearlman, MD, PhD, ME, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Ronald J Oudiz, MD, Director of Pulmonary Hypertension, Associate Professor, Department of Medicine, Division of Cardiology, Harbor-UCLA Medical Center, David Geffen School of Medicine at UCLA
Ronald J Oudiz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Heart Association
Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

George A Stouffer III, MD, Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center
George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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